Cattle trypanosomosis: the diversity of …web.oie.int/boutique/extrait/24auty587598.pdfCattle trypanosomosis: the diversity of trypanosomes and implications for disease epidemiology

Cattle trypanosomosis: the diversity of trypanosomes and implications for disease epidemiology and control

H. Auty (1), S.J. Torr (2), T. Michoel (3), S. Jayaraman (3) & L.J. Morrison (3)*

(1) SRUC, Epidemiology Unit, Drummondhill, Stratherrick Road, Inverness IV2 4JZ, United Kingdom(2) Liverpool School of Tropical Medicine, Pembroke Place, Liverpool L3 5QA, United Kingdom(3) Roslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian EH25 9RG, United Kingdom*Corresponding author: [email protected]

SummaryTrypanosomosis is one of the most significant infectious threats to cattle in sub-Saharan Africa, and one form has also spread to Asia and South America. The disease is caused by a complex of trypanosome species, and the species and strain of parasite can have a profound influence upon the epidemiology of the host–parasite–vector relationships, the severity and course of infection, and, consequently, the implementation and development of control methods. This review will summarise our current knowledge of the relationship between trypanosome species/genotype and the phenotype of disease in cattle, and the implications that this has for ongoing efforts to develop diagnostics, drugs and vaccines for the control of cattle trypanosomosis.

KeywordsAfrican animal trypanosomosis – Cattle – Diversity – Trypanosoma brucei – Trypanosoma brucei evansi – Trypanosoma congolense – Trypanosoma vivax – Trypanosome – Tsetse fly – Vector-borne disease.

Rev. Sci. Tech. Off. Int. Epiz., 2015, 34 (2), 587-598

IntroductionAfrican animal trypanosomosis (AAT) remains one of the biggest infectious disease constraints to productive livestock rearing in sub-Saharan Africa – recent estimates suggest a cost to East Africa alone of US$4.5 billion (1). AAT is also becoming increasingly prevalent beyond its traditionally defined realm and is an established threat to animal health in South America and Asia. This article will summarise our current understanding of the causative agents of AAT and reviews how their distinct epidemiological factors relate to particular threats to animal health and the concomitant different requirements for control. (The clinical disease is adequately reviewed elsewhere [2, 3], and the biology and control of the tsetse fly vector are discussed in other papers in the current issue [4, 5].) The authors also highlight recent initiatives in the development of novel diagnostic tools and therapeutic and prophylactic compounds, which are sorely required to advance the control of AAT.

Much trypanosome research has focused on Trypanosoma brucei, subspecies of which (T. b. gambiense and T. b. rhodesiense) cause human African trypanosomosis (HAT) (6). Trypanosoma brucei has also proved a tractable laboratory model, and the combination of relevance to human disease and utility in the laboratory means that the development of tools and understanding for the main livestock pathogens in sub-Saharan Africa, T. congolense and T. vivax, has lagged significantly behind that of T. brucei. There has also been a degree of assumption by many trypanosome researchers that findings in T. brucei will translate directly to T. congolense and T. vivax. However, it is becoming increasingly clear that these organisms are different in many aspects of their biology (e.g. 7, 8), so research on the causative agents of AAT should now become a funding priority. Moreover, outside Africa, T. brucei evansi, the mechanically transmitted variant of T. brucei, is an increasingly significant pathogen of cattle and other animals in South America and Asia. There has been a renewed focus of research on all three of these livestock trypanosomes, and sequenced reference genomes of T. brucei, T. congolense

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and T. vivax are now available (7, 9, 10) (www.tritrypdb.org). Additionally, in vitro systems of culture and genetic manipulation for both T. congolense and T. vivax have recently been developed (11, 12). Consequently, we are entering an era in which an increased focus of research on the relevant trypanosome species will lead to a better understanding of the roles of different trypanosome species and genotypes in livestock disease and, ultimately, to the development of better tools and strategies to improve the health and productivity of livestock.

Trypanosome species of relevance to cattleThe main causative agents of disease in livestock are T. congolense and T. vivax in cattle, and there is some contribution to disease by T. brucei, in particular the subspecies T. b. evansi (in horses, camels, water buffalo and cattle) and T. b. equiperdum (in horses and donkeys) (13). Trypanosomes are spread by the bite of infected tsetse flies (Glossina species) in sub-Saharan Africa and their distribution is largely tied to that of the insect vector. However, T. congolense has been shown in experimental situations to be capable of mechanical transmission by biting flies (14), and T. b. evansi and T. vivax have both particularly adapted to non-cyclical mechanical transmission by other biting flies (e.g. Tabanids and Stomoxyines). Trypanosoma brucei equiperdum is venereally transmitted and appears to be restricted to equidae. The transmission modes of T. b. evansi and T. vivax have enabled their spread beyond the ‘traditional’ tsetse belt of sub-Saharan Africa; T. vivax is now established across much of South America in cattle (15), and T. b. evansi is a threat to cattle, water buffalo and camels across Asia and South America (16, 17). Trypanosoma brucei populations in cattle are also a reservoir for the human-infective subspecies T. b. rhodesiense, and movement of cattle has been implicated in the spread and seeding of human disease outbreaks caused by this pathogen (18). Other species, such as T. simiae and T. godfreyi (and, rarely, T. suis) have been diagnosed in livestock, but their precise role in clinical disease in livestock, and cattle in particular, remains unclear. Indeed, as will be summarised in the following section, our understanding of the link between trypanosome species/genotype and disease phenotype in livestock, and therefore of the relative importance to the syndrome of cattle trypanosomosis, is lagging behind much recent progress in the ability to diagnose and identify the species and genotype of trypanosomes that are found in animals (19, 20, 21).

Trypanosoma congolense

Trypanosoma congolense is the main causative agent of AAT in sub-Saharan Africa. It is comprised of genetically divergent subgroups, namely ‘Savannah’, ‘Forest’ and ‘Kilifi’, which

were initially identified on the basis of isoenzyme analysis (22, 23, 24). This classification has subsequently been validated by a range of other genetic markers (e.g. 25, 26). Trypanosoma congolense Savannah, the most widespread subgroup geographically, is found over much of sub-Saharan Africa (Fig. 1) and is considered the main pathogen of cattle. The Savannah group can be further clustered into East and West African groups on the basis of genetic similarity (23). Trypanosoma congolense Forest is distributed mainly in Western African forest biotopes, although polymerase chain reaction (PCR) assays have shown that it also exists at low levels in Tanzania and Zambia (e.g. 27, 28, 29). The distribution of T. congolense Forest seems to be linked with that of the tsetse fly vector Glossina palpalis (30, 31, 32), perhaps explaining its distribution across the continent (33). Trypanosoma congolense Kilifi is largely restricted to East and Southern Africa, but has also been diagnosed by isoenzyme analysis and PCR in Cameroon and Côte d’Ivoire (31, 34, 35). The detection of T. congolense Forest and T. congolense Kilifi in the geographical ‘outliers’ described above has mostly been undertaken in tsetse flies (but also in pigs and wildlife [27, 35]) and so our understanding of the relationship between the presence of the organisms and infection/disease in cattle is currently unclear. The patchiness of these data suggest that more widespread epidemiological surveying of mammalian and vector hosts and the application of sensitive diagnostic tools will add significantly to the currently defined geographic range (and potential contribution to disease) of T. congolense Forest and T. congolense Kilifi in particular.

The limited data available suggest that T. congolense Savannah is significantly more genetically diverse (26, 36) than T. congolense Forest (26, 37), with consequent implications for potential diversity of phenotypes within subgroups. Data on the relationship between parasite genotype and the phenotype of disease severity in the mammalian host are currently in short supply, but when cattle were experimentally infected with two clones of each T. congolense subgroup, it was demonstrated that T. congolense Savannah infections resulted in consistently higher parasitaemia, more severe anaemia (as measured by lower packed cell volume) and higher levels of mortality than infections with T. congolense Forest or Kilifi, both of which resulted in milder clinical symptoms and recovery (38). These experimental data are therefore consistent with epidemiological data indicating that T. congolense Savannah is the main pathogen of clinical concern for cattle. However, much work remains to be done to unravel the implications for disease spread and epidemiology, variation in disease severity and diagnosis of the different T. congolense subgroups. Additionally, the relationship between the diverse T. congolense subgroups and the variety of tsetse vector species, and the impact that these relationships may have upon the epidemiology of disease (and therefore control), is a potentially important factor that deserves more attention.

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Trypanosoma vivax

Trypanosoma vivax is spread across much of sub-Saharan Africa, and has also established in South America (15) (Fig. 2). Transmission is both mechanical and cyclical in sub-Saharan Africa but only mechanical in South America, where the tsetse fly vector is absent. Despite the wide distribution and economic importance of T. vivax it is much the most neglected trypanosome with respect to research and development of species-specific tools (39); this is largely because T. vivax is notoriously difficult to work with in the laboratory, with very few strains growing

in rodents and, until recently, no strain being adapted to grow reproducibly in vitro. However, recent developments in culturing and genetic manipulation have opened up the ability to advance our knowledge of this parasite (12). Among the tsetse-transmitted trypanosomes, T. vivax is phylogenetically the most distinct (19, 39, 40, 41), which is reflected in its divergence in, for example, variant surface glycoprotein (VSG) repertoire composition, structure and usage compared to T. congolense and T. brucei (7, 9). Genetic analyses using isoenzymes and a variety of DNA markers indicate that T. vivax can be separated into two groups, which largely correspond to geographic location, i.e. an East

T. congolense Savannah, Forest & Kilifi

T. congolense Savannah & Forest

T. congolense Savannah & Kilifi

T. congolense Savannah

T. congolense Forest

T. congolense subspecies undefined

T. congolense inferred

Fig. 1 Distribution of Trypanosoma congolense and subgroupsThe map shows distribution of T. congolense, including, where available, confirmed presence of each of the three subgroups Savannah, Forest and Kilifi (detected by isoenzyme or PCR analysis). For some countries data are not present at the subgroup level, and for some countries data at the species level are missing and presence is inferred. It should be noted that distribution of T. congolense in some of the indicated countries is very limited (e.g. South Africa, Namibia and Botswana) and is directly related to the limited distribution of the tsetse vector. Additionally, the data in many countries are from a limited baseline, and the absence of, for example, a particular subgroup may merely indicate lack of detection, not necessarily absence of the parasite. Country data were generated by searching PubMed for ‘congolense and country name’


African group and a West African group (42, 43). There is some evidence to suggest that West African T. vivax is more pathogenic to cattle than East African T. vivax (39), but in common with the other trypanosome species of importance to cattle, this link between trypanosome genotype and disease severity in the mammalian host remains unclear. There have also been several sporadic reports, mainly from East Africa, of T. vivax infections that result in a severe haemorrhagic syndrome in cattle (44, 45, 46, 47) – isoenzyme analysis provided some suggestion that the T. vivax strains associated with this severe disease were distinct, and this hypothesis also requires further confirmation (42). The genetics of South American T. vivax have been examined, and its very limited diversity is consistent with a West African T. vivax strain being introduced on a limited number of occasions at the turn of the 20th Century, presumably through the import of infected cattle (48, 49). Although studies indicate that T. vivax reproduces clonally (50) and therefore may be expected to be limited in diversity, at least at the local level, data suggest that there is likely to be a range of genetically distinct T. vivax populations, the implications of which are currently unclear. Several studies have identified distinct

T. vivax isolates by examining ribosomal 18S sequences isolated from tsetse flies and wildlife hosts (51, 52). While we do not know the relevance of these divergent T. vivax genotypes to disease in cattle or other domestic animals, importantly it was observed that current T. vivax molecular diagnostic tools do not recognise these genotypes (52), and thus current screening would not detect them. Therefore, these latter studies indicate the importance of understanding the diversity of T. vivax and developing tools that will detect the different genotypes, enabling a more accurate assessment of the importance of T. vivax to livestock health.

Trypanosoma brucei subspecies

Trypanosoma brucei sensu lato are often detected in cattle, but their relationship to clinical disease is not straightforward and seems to be dependent upon several factors, including genotype of the parasite and epidemiological setting. Trypanosoma brucei exists as a complex of subspecies and variants. Trypanosoma brucei brucei is widespread across sub-Saharan Africa and is found in both wild animal and livestock hosts, but current perception is that T. b. brucei

T. vivax

T. vivax inferred

Fig. 2 Distribution of Trypanosoma vivaxFor some countries data were not available and presence has been inferred. Country data were generated by searching PubMed for ‘vivax and country name’


does not contribute significantly to cattle disease in sub-Saharan Africa (e.g. 53). However, cattle have been shown to play a role as reservoir hosts in the dissemination of the human parasite T. b. rhodesiense in Uganda (54, 55) (but not of T. b. gambiense [56]), and therefore diagnosis and control of T. brucei in cattle populations may well have important implications for human health in T. b. rhodesiense-endemic areas. Trypanosoma brucei evansi is a mutant of T. brucei that has adapted to mechanical transmission, and has therefore been able to spread beyond the tsetse belt of sub-Saharan Africa throughout much of North Africa, South and Eastern Asia and South America (Fig. 3). The process of adapting to mechanical transmission has occurred more than once (i.e. T. b. evansi does not represent a single clonal lineage [13, 57]), and during each adaptation event T. b. evansi has lost all or some elements of the kinetoplast (the equivalent of the mitochondrion), which is required to be active during cyclical transmission in the tsetse fly vector in order to exploit the predominant energy source in the fly midgut (proline). In contrast, the kinetoplast is not active or required in the mammal due to the abundance of glucose in blood. The kinetoplast is also involved in the life cycle stage differentiation of T. brucei that occurs in the mammalian host, whereby the cells differentiate from the multiplicative long slender form into the arrested short stumpy life cycle

stage that is pre-adapted to the tsetse fly vector (58). This differentiation regulates the parasitaemia in T. brucei infections and the loss of this differentiation ability has been speculated to lead to increased parasitaemias in T. b. evansi- infected hosts that may facilitate mechanical transmission (57, 59). It also potentially explains, at least partially, the increased virulence of T. b. evansi in cattle compared to T. b. brucei. Additionally, experimental work using the rodent model of the malaria parasite Plasmodium has demonstrated that there is a ‘resetting’ of virulence when parasites transmit cyclically through the insect vector (60), in contrast to increasing virulence with serial passage in the absence of cyclical transmission. Increasing virulence is also observed with serial passage in vitro or in mice with T. brucei, and this correlates with a concomitant loss of transmissibility and increased virulence (61, 62). This suggests that transmission through the vector may play a crucial role in limiting the pathogenicity of T. b. brucei, whereas the serial mechanical transmission of T. b. evansi may contribute to its increased pathogenicity. Trypanosoma brucei infection biology is also characterised by its extravasation as infections progress, leading to significant invasion of multiple tissues and consequent tissue-specific pathologies (e.g. brain and heart involvement in HAT infections [63, 64]). While this is a feature of infections in equidae, particularly with respect

T.b. evansi

T.b. evansi inferred

T.b. evansi single outbreak

Fig. 3 Distribution of Trypanosoma brucei evansiFor some countries data were not available and presence has been inferred. Cases in France and mainland Spain have been isolated outbreaks which have since been eradicated (although T. b. evansi persists in camels on the Canary Islands). Data for several countries relate to infection in non-bovine hosts (e.g. camels, equidae), but these data have been included in this figure as infection in these hosts presents a risk for other animals and therefore the presence of infection in cattle cannot be ruled out. Country data were generated by searching PubMed for ‘evansi and country name’


to neurological signs in horses infected with T. brucei and T. b. evansi (65, 66, 67), neurological signs do not seem to be a particularly notable clinical feature in infected cattle.

Trypanosoma b. evansi is largely considered a pathogen of camels and equidae in North Africa and the Middle East, but in South America and East Asia it is a pathogen that has a significant impact upon the cattle and water buffalo industries of these regions (16, 68, 69). It is not considered to be a prevalent pathogen in sub-Saharan Africa, but this may in fact be due to the current inability to differentiate T. b. evansi from T. b. brucei in the event of co-infections where both (as well as possibly T. b. equiperdum) may be present (70). Indeed, diagnosis of T. b. evansi still largely relies upon the RoTat 1.2 VSG, and it is clear that variants of T. b. evansi exist that do not express this gene (71) (T. b. evansi ‘strain B’) – the reliance on RoTat 1.2 as a diagnostic has undoubtedly meant that the presence of non-RoTat 1.2 T. b. evansi is under-diagnosed (72).

Advances in diagnosis and treatmentAs can be seen by the discussion above, bovine trypanosomosis is a disease caused by multiple parasite species, and the subgroup of these species may have implications for the epidemiology, severity and management of the disease. Our understanding of the epidemiology of trypanosomosis is therefore reliant upon accurate diagnosis and distinction between the species. Diagnosis in the field is currently still largely reliant upon clinical signs, with anaemia in endemic areas being an indicator for treatment (e.g. 73). Microscopy is also widely used as the ‘gold standard’ diagnostic, but it is a technique which clearly has sensitivity issues. There is a significant need for a test that is applicable ‘pen-side’ and that is affordable to smallholder farmers in endemic regions. While there have been significant advances in the development of molecular (primarily DNA-based) markers to enable differentiation of species and subgroups, the application of standard molecular techniques such as PCR is clearly impractical in the field. However, recent molecular advances have the potential to facilitate the development of tests that are applicable to field settings, in particular those based on loop-mediated isothermal amplification (LAMP), which only requires one water bath at a particular temperature and for which user-friendly fluorescent readouts that do not require technology have been developed (74). The LAMP technology has been particularly developed by the Foundation for Innovative Diagnostics (FIND) (www.finddiagnostics.org) and partners, who are in the advanced stages of working towards a diagnostic kit that is applicable to detection of HAT in the field. The resources have been developed for all three livestock species to allow this

potential to be realised for AAT (e.g. 72, 75, 76). Therefore, the platform exists for these diagnostic tools to be applicable in the field in the relatively near future.

Clearly, the power of any diagnostic relies upon identifying the appropriate antigen or antibody that will provide the necessary specificity and sensitivity. PCR or DNA-based tests such as LAMP provide the highly desirable ability to directly detect the pathogen, but often parasitaemias can be very variable, and therefore appropriate serological tests would also be useful. Serological tests based on immunodominant antigens for trypanosomes almost inevitably involve the VSG, because the VSG is particularly immunogenic and is expressed at a significantly higher level than any other trypanosome protein (although interestingly in T. vivax this may not be true to the same extent [39, 77]). However, the variable nature of the VSG repertoire within and between trypanosome strains makes it a somewhat problematic tool for diagnostics. Although the VSG can be a useful diagnostic substrate for clonal trypanosome species/strains in which there is limited diversity and relative conservation of the content and usage of the VSG repertoire (e.g. VSGs are the target for the CATT test for T. b. gambiense [78] and RoTat 1.2-based diagnosis of T. b. evansi), such an approach is unlikely to be applicable to T. congolense and T. brucei in particular. In theory a VSG-based test may be more suited to the detection of T. vivax, but the problems with such tests for T. vivax would be much the same as those surrounding the RoTat 1.2-based test for T. b. evansi. The overall within-species diversity in both T. congolense and T. vivax probably means that a ‘catch-all’ diagnostic test that is based on VSGs is unlikely to be successful. Recent advances and non-biased approaches do show some promise for HAT (e.g. 79), particularly as they have identified non-varying surface antigens as potential diagnostic substrates that will potentially avoid many of the pitfalls associated with VSGs described above. A different methodology that merits continued investment is the identification of biomarkers, which are measurable substances or processes that indicate a biological status, for example, active infection. Biomarkers may provide a route to obviating the problems inherent in antibody-based tests with respect to diagnosing active infections, given the persistence of antibodies after removal of the pathogen. Efforts have been made to define biomarkers of T. b. gambiense infections in humans, with some promising results (e.g. neopterin in cerebrospinal fluid as a diagnostic indicator of Stage 2 T. b. gambiense HAT [80]). The availability of sequenced genomes combined with current technologies such as the ability to measure, for example, in-depth gene expression and metabolite levels in infected animals, means that the identification of biomarkers for cattle trypanosomosis is a viable proposition.

The VSG repertoire of these organisms and their antigenic variation also underpin why a protective vaccine is extremely unlikely and rarely discussed as a possibility, particularly if


based upon the immunodominant VSG. However, potential still remains for anti-disease vaccines, whereby targeting an appropriate trypanosome protein that mediates pathology can reduce the severity of clinical signs. This has been trialled in cattle with T. congolense Cathepsin L, where subunit vaccines reduced disease severity (as measured by weight gain and rate of anaemia recovery) in comparison with unvaccinated controls (81), providing proof of principle. Such approaches have also been undertaken using T. congolense trans-sialidases (TcoTS; albeit in mice), where immunisation with two TS variants (TcoTS-A1 and TcoTS-Like2) resulted in reduced severity and an increased rate of recovery from anaemia in vaccinated animals relative to controls (82). Orthologues of these proteins have also been shown to be virulence factors in T. vivax (again in mice [83]), and so studies such as these indicate the potential for anti-disease vaccination as a tool in the armoury to combat bovine trypanosomosis.

The control of bovine trypanosomosis is currently entirely reliant upon either drug treatment or vector control (the latter is covered in detail elsewhere in this issue [4, 5]). Currently, two drugs are used for the majority of treatments for cattle trypanosomosis: diminazene aceturate and isometamidium chloride. These drugs are now over 50 years old, and there are increasing reports of treatment failure that are likely to be due to drug resistance (84). The combination of the reliance upon these two drugs, their widespread use over decades, and the variable quality and frequent counterfeiting of the compounds (which undoubtedly leads to under-dosing) is a recipe for there imminently being no useful compounds for bovine trypanosomosis. Accordingly, the search for new therapeutic (and ideally prophylactic) compounds is an urgent priority. Several efforts are underway to develop new compounds for both HAT and AAT, and this, combined with recently described developments in compound identification (e.g. 85), means that a compound(s) to target both diseases will hopefully become available in the next decade.

Conclusion‘Bovine trypanosomosis’, rather than being a single clinical entity, comprises a complex of clinical diseases that differ in epidemiology and clinical presentation. Much of this complexity derives from the diversity of the parasites themselves, which then interacts with host and vector diversity to create an intricate balance of inputs that contribute to clinical severity and infection outcome. While parasite diversity may at first seem a rather esoteric topic for a review on bovine trypanosomosis, it has

important implications for treatment and diagnosis, and for prospects of developing tools to manage the disease. This can perhaps be exemplified by drug resistance to diamidine compounds such as diminazene aceturate; as outlined above, this drug is very widely used in cattle and resistance is arising. In T. brucei the drug is taken up into the trypanosomes predominantly by one transporter, T. brucei adenosine transporter 1 (TbAT1) (86). Consequently, resistant T. brucei parasites tend to display a mutation in this gene and resistance is due to reduced uptake of the drug (87). Therefore, understanding the mechanism of uptake helps us understand the underlying mechanism of resistance and will inform the subsequent development of novel compounds to target the parasite (e.g. ideally a new drug will utilise a different uptake route to avoid cross-resistance). However, when the genome of T. congolense was analysed, it became evident that T. congolense does not have a gene that corresponds to TbAT1 (8, 9). Therefore, the drug must be entering the parasites through a different route, and the primary mechanism of resistance will also be different. Hence, understanding the basic differences between the trypanosome species will help us understand some fundamental aspects of (i) how the parasite diversity impacts upon traits that determine the future development of tools such as drugs, and (ii) how the deployment of such tools impacts upon the trypanosome population (e.g. rate and mechanism of drug resistance development). Therefore, to tackle bovine trypanosomosis in a holistic manner, it is vital that we continue to develop the basic understanding of the infection biology of what are a range of very different parasites, as this can then feed into rational development of tools that will appropriately target the diverse species of trypanosomes outlined above.

AcknowledgementsLM is a Royal Society University Research Fellow (UF090083). LM, TM & SJ are supported by the core funding of the Roslin Institute provided by the Biotechnology and Biological Sciences Research Council (BBSRC). LM, ST & HA are funded by a BBSRC ZELS (Zoonoses and Emerging Livestock Systems) grant (BB/L019035/1).


Trypanosomose bovine: la diversité des trypanosomes et ses conséquences sur l’épidémiologie de la maladie et sur son contrôle

H. Auty, S.J. Torr, T. Michoel, S. Jayaraman & L.J. Morrison

RésuméLa trypanosomose constitue l’une des principales maladies infectieuses menaçant la santé des bovins d’Afrique subsaharienne ; l’une des formes de cette maladie s’est également propagée en Asie et en Amérique latine. La maladie est causée par un complexe d’espèces de trypanosomes. L’espèce et la lignée du parasite influent beaucoup sur l’épidémiologie des interactions hôte-parasite-vecteur, sur la gravité et l’évolution de l’infection et, à terme, sur la conception et le déroulement des méthodes de lutte. Les auteurs font le point sur l’état actuel des connaissances concernant les relations entre l’espèce et le génotype des trypanosomes, d’une part, et le phénotype de la maladie chez les bovins, d’autre part, et soulignent les conséquences de ces interactions pour les travaux en cours visant à développer des tests de diagnostic, des médicaments et des vaccins pour lutter contre la trypanosomose bovine.

Mots-clésBovin – Diversité – Glossine – Maladie à transmission vectorielle – Trypanosoma brucei – Trypanosoma brucei evansi – Trypanosoma congolense – Trypanosoma vivax – Trypanosome – Trypanosomose animale africaine.

Tripanosomosis bovina: diversidad de tripanosomas y su influencia en la epidemiología y el control de la enfermedad

H. Auty, S.J. Torr, T. Michoel, S. Jayaraman & L.J. Morrison

ResumenLa tripanosomosis es una de las infecciones más importantes que amenazan al ganado vacuno en el África subsahariana, y ahora una de sus formas se ha extendido también a Asia y Sudamérica. La causa de la enfermedad es un complejo de especies de tripanosoma. La especie y cepa del parásito pueden influir sobremanera en la epidemiología de la relación hospedador-parásito-vector, en la gravedad y evolución de la infección y, por ende, en los métodos de lucha que se puedan definir y aplicar. Tras resumir lo que hasta ahora se sabe de la relación entre la especie y el genotypo del tripanosoma y el fenotipo de la enfermedad en los bovinos, los autores explican la influencia que ello tiene en las actividades en curso para definir métodos de diagnóstico y obtener fármacos y vacunas que ayuden a luchar contra la tripanosomosis bovina.

Palabras claveDiversidad – Enfermedad transmitida por vectores – Ganado vacuno – Mosca tse-tsé – Tripanosoma – Tripanosomosis animal africana – Trypanosoma brucei – Trypanosoma brucei evansi – Trypanosoma congolense – Trypanosoma vivax.


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